Characterizing and Predicting Outcomes of Communication Delays in Infants and Toddlers: Implications for Clinical Practice

Purpose: This article focuses on using currently available data to assist speech-language pathologists (SLPs) in making decisions regarding a child\u27s eligibility and considerations for recommended dosage of early intervention (El) services. Method: Literature describing the characteristics of infants and toddlers who are likely recipients of El services was reviewed. Results: Current literature provides information that can be used to inform clinical decisions for infants and toddlers with established medical conditions, as well as those with risk factors, for oral language, communication, and subsequent literacy disabilities. This information is summarized. Conclusion: Extant literature suggests that El makes a critical difference in the developmental course of communication as well as in other learning domains for children with a variety of established conditions. The literature also provides guidance to SLPs who must evaluate and weigh risk factors for children with less clear eligibility for services

Immunological aspects of the tumor microenvironment and epithelial-mesenchymal transition in gastric carcinogenesis

Infection with Helicobacter pylori, a Gram-negative, microaerophilic pathogen often results in gastric cancer in a subset of affected individuals. This explains why H. pylori is the only bacterium classified as a class I carcinogen by the World Health Organization. Several studies have pinpointed mechanisms by which H. pylori alters signaling pathways in the host cell to cause diseases. In this article, the authors have reviewed 234 studies conducted over a span of 18 years (2002–2020). The studies investigated the various mechanisms associated with gastric cancer induction. For the past 1.5 years, researchers have discovered new mechanisms contributing to gastric cancer linked to H. pylori etiology. Alongside alteration of the host signaling pathways using oncogenic CagA pathways, H. pylori induce DNA damage in the host and alter the methylation of DNA as a means of perturbing downstream signaling. Also, with H. pylori, several pathways in the host cell are activated, resulting in epithelial-to-mesenchymal transition (EMT), together with the induction of cell proliferation and survival. Studies have shown that H. pylori enhances gastric carcinogenesis via a multifactorial approach. What is intriguing is that most of the targeted mechanisms and pathways appear common with various forms of cancer

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Mechanisms of the Epithelial-Mesenchymal Transition and Tumor Microenvironment in Helicobacter pylori-Induced Gastric Cancer

Helicobacter pylori (H. pylori) is one of the most common human pathogens, affecting half of the world's population. Approximately 20% of the infected patients develop gastric ulcers or neoplastic changes in the gastric stroma. An infection also leads to the progression of epithelial-mesenchymal transition within gastric tissue, increasing the probability of gastric cancer development. This paper aims to review the role of H. pylori and its virulence factors in epithelial-mesenchymal transition associated with malignant transformation within the gastric stroma. The reviewed factors included: CagA (cytotoxin-associated gene A) along with induction of cancer stem-cell properties and interaction with YAP (Yes-associated protein pathway), tumor necrosis factor α-inducing protein, Lpp20 lipoprotein, Afadin protein, penicillin-binding protein 1A, microRNA-29a-3p, programmed cell death protein 4, lysosomal-associated protein transmembrane 4β, cancer-associated fibroblasts, heparin-binding epidermal growth factor (HB-EGF), matrix metalloproteinase-7 (MMP-7), and cancer stem cells (CSCs). The review summarizes the most recent findings, providing insight into potential molecular targets and new treatment strategies for gastric cancer

Care pathways at end-of-life for cancer decedents : registry based analyses of the living situation, healthcare utilization and costs for all cancer decedents in Norway in 2009-2013 during their last 6 months of life

Background: Research on end-of-life care is often fragmented, focusing on one level of healthcare or on a particular patient subgroup. Our aim was to describe the complete care pathways of all cancer decedents in Norway during the last six months of life. Methods: We used six national registries linked at patient level and including all cancer decedents in Norway between 2009-2013 to describe patient use of secondary, primary-, and home- and community-based care. We described patient’s car pathway, including patients living situation, healthcare utilization, and costs. We then estimated how cancer type, individual and sociodemographic characteristics, and access to informal care influenced the care pathways. Regression models were used depending on the outcome, i.e., negative binomial (for healthcare utilization) and generalized linear models (for healthcare costs). Results: In total, 52,926 patients were included who died of lung (16%), colorectal (12%), prostate (9%), breast (6%), cervical (1%) or other (56%) cancers. On average, patients spent 123 days at home, 24 days in hospital, 16 days in short-term care and 24 days in long-term care during their last 6 months of life. Healthcare utilization increased towards end-of-life. Total costs were high (on average, NOK 379,801). 60% of the total costs were in the secondary care setting, 3% in the primary care setting, and 37% in the home- and community-based care setting. Age (total cost-range NOK 361,363-418,618) and marital status (total cost-range NOK354,100-411,047) were stronger determining factors of care pathway than cancer type (total cost-range NOK341,318- 392,655). When patients died of cancer types requiring higher amounts of secondary care (e.g., cervical cancer), there was a corresponding lower utilization of primary, and home- and community-based care, and vice versa. Conclusion: Cancer patient’s care pathways at end-of-life are more strongly associated with age and access to informal care than underlying type of cancer. More care in one care setting (e.g., the secondary care) is associated with less care in other settings (primary- and home- and community based care setting) as demonstrated by the substitution between the different levels of care in this study. Care at end-of-life should therefore not be evaluated in one healthcare level alone since this might bias results and lead to suboptimal priorities.publishedVersionPeer reviewe

Association between the c.*229C>T polymorphism of the topoisomerase IIb binding protein 1 (TopBP1) gene and breast cancer

Topoisomerase IIb binding protein 1 (TopBP1) is involved in cell survival, DNA replication, DNA damage repair and cell cycle checkpoint control. The biological function of TopBP1 and its close relation with BRCA1 prompted us to investigate whether alterations in the TopBP1 gene can influence the risk of breast cancer. The aim of this study was to examine the association between five polymorphisms (rs185903567, rs116645643, rs115160714, rs116195487, and rs112843513) located in the 30UTR region of the TopBP1 gene and breast cancer risk as well as allele-specific gene expression. Five hundred thirty-four breast cancer patients and 556 population controls were genotyped for these SNPs. Allele-specific Top- BP1 mRNA and protein expressions were determined by using real time PCR and western blotting methods, respectively. Only one SNP (rs115160714) showed an association with breast cancer. Compared to homozygous common allele carriers, heterozygous and homozygous for the T variant had significantly increased risk of breast cancer (adjusted odds ratio = 3.81, 95 % confidence interval: 1.63–8.34, p = 0.001). Mean TopBP1 mRNA and protein expression were higher in the individuals with the CT or TT genotype. There was a significant association between the rs115160714 and tumor grade and stage. Most carriers of minor allele had a high grade (G3) tumors classified as T2-T4N1M0. Our study raises a possibility that a genetic variation of TopBP1 may be implicated in the etiology of breast cancer

Gene expression of O-GlcNAc cycling enzymes in human breast cancers

O-GlcNAcylation is an abundant, dynamic, and inducible posttranslational modification in which single β-N-acetylglucosamine residues are attached by O-glycosidic linkage to serine or treonine residues. It is suggested that abnormally regulated O-GlcNAcylation may contribute to the pathology of cancer. Cycling of O-GlcNAc residues on intracellular proteins is controlled by two enzymes, O-GlcNAc transferease (OGT), which catalyses the addition of O-GlcNAc residues and nucleocytoplasmic β-N-acetylglucosaminidase (O-GlcNAcase; encoded by MGEA5 gene), an enzyme involved in the removal of O-GlcNAc. In this study, relationship between the mRNA expressions of genes coding O-GlcNAc cycling enzymes in breast ductal carcinomas and clinicopathological parameters were analyzed. The results showed that poorly differentiated tumors (grade II and III) had significantly higher OGT expression than grade I tumors. Contrary, MGEA5 transcript levels were significantly lower in grade II and III in comparison with grade I tumors. The Spearman rank correlation showed the expressions of OGT and MGEA5 in breast cancer was negatively correlated (r = −0.430, P = 0.0002). Lymph node metastasis status was significantly associated with decreased MGEA5 mRNA expression. This result suggests that elevation in O-GlcNAc modification of proteins may be implicated in breast tumor progression and metastasis

Dementia as a determinant of social and health service use in the last two years of life 1996-2003

<p>Abstract</p> <p>Background</p> <p>Dementia is one of the most common causes of death among old people in Finland and other countries with high life expectancies. Dementing illnesses are the most important disease group behind the need for long-term care and therefore place a considerable burden on the health and social care system. The aim of this study was to assess the effects of dementia and year of death (1998-2003) on health and social service use in the last two years of life among old people.</p> <p>Methods</p> <p>The data were derived from multiple national registers in Finland and comprise all those who died in 1998, 2002 or 2003 and 40% of those who died in 1999-2001 at the age of 70 or over (n = 145 944). We studied the use of hospitals, long-term care and home care in the last two years of life. Statistics were performed using binary logistic regression analyses and negative binomial regression analyses, adjusting for age, gender and comorbidity.</p> <p>Results</p> <p>The proportion of study participants with a dementia diagnosis was 23.5%. People with dementia diagnosis used long-term care more often (OR 9.30, 95% CI 8.60, 10.06) but hospital (OR 0.33, 95% CI 0.31, 0.35) and home care (OR 0.50, 95% CI 0.46, 0.54) less often than people without dementia. The likelihood of using university hospital and long-term care increased during the eight-year study period, while the number of days spent in university and general hospital among the users decreased. Differences in service use between people with and without dementia decreased during the study period.</p> <p>Conclusions</p> <p>Old people with dementia used long-term care to a much greater extent and hospital and home care to a lesser extent than those without dementia. This difference persisted even when controlling for age, gender and comorbidity. It is important that greater attention is paid to ensuring that old people with dementia have equitable access to care.</p